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ShcA expression in podocytes is dispensable for glomerular development but its upregulation is associated with kidney

Claire E Martin1, Nina Jones1

  • 1Department of Molecular and Cellular Biology, University of Guelph Guelph, ON, Canada.

American Journal of Translational Research
|September 20, 2021
PubMed

Insights

ShcA (SHC1) protein is not essential for normal kidney function in mice. However, increased ShcA expression in podocytes is linked to kidney disease and proteinuria.

Area of Science:

  • Molecular biology
  • Nephrology
  • Cell signaling

Background:

  • ShcA (SHC1) is a key phosphotyrosine adaptor protein with vital cellular signaling roles.
  • Embryonic ShcA loss is lethal; aberrant expression is linked to various diseases.
  • ShcA is highly expressed in developing glomeruli and upregulated in podocytes during kidney injury and disease.

Purpose of the Study:

  • To investigate the in vivo role of ShcA specifically within kidney podocytes.

Main Methods:

  • Selective deletion of all ShcA isoforms in mouse podocytes using the Cre/lox system (Nphs2 promoter).
  • Confirmation of ShcA deletion via immunostaining.
  • Assessment of urinary albumin, glomerular morphology (light and electron microscopy), and SHC1 mRNA levels in human renal disease (Nephroseq database).

Main Results:

  • Mice lacking podocyte ShcA showed normal development and no overt renal impairment up to one year of age.
  • Increased ShcA mRNA expression in human kidneys correlated with proteinuria and reduced glomerular filtration rate.

Conclusions:

  • Podocyte ShcA is dispensable for normal kidney function.
  • Upregulation of ShcA is associated with kidney disease, suggesting a role in disease pathogenesis rather than normal physiology.
Abstract

Keywords:
NephroseqShcAglomerulusknockout micepodocyte

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